Traumatic brain injury (TBI) is the leading cause of death and morbidity in young, otherwise healthy populations and results in an enormous social and economic cost. Although commonly used clinical markers are statistically linked with gross functioning in large studies, they are less useful in predicting cognitive functioning in individual patients. Similarly, although conventional neuroimaging studies can guide acute clinical management, outcome prediction is unreliable, particularly at early stages of injury resolution. Preliminary data from our laboratory show that neurometabolite markers of brain cellular injury measured by non-invasive magnetic resonance spectroscopy are strongly correlated with cognitive function and outcome. Further, our data show that certain anatomic locations are more intensely injured than others (i.e., anterior brain more than posterior), and that gray matter neurometabolites predict cognitive outcome more reliably than white matter, suggesting tissue heterogeneity of response to TBI. We also show that recovery of these neurometabolites is temporarily associated with cognitive improvement. We propose a novel approach for assessment and study of TBI using quantitative magnetic resonance spectroscopic imaging (SI) and MRI to quantify cellular brain injury. These measurements of N- acetylaspartate, choline-containing compounds, and water relaxation times are a powerful new tool for prediction of brain function and outcome. Using these neurometabolite markers of injury in normal-appearing (by MRI) brain, we aim to determine whether specific patterns-anatomic and/or tissue-type of injury are associated with specific forms of cognitive dysfunction. Magnetic resonance spectroscopic imaging offers a robust new tool to investigate the metabolic integrity of the neuron following TBI, and may provide new insight into clinical management, patient heterogeneity, prediction of outcome, and the determination of effectiveness of therapeutic options.